serine/threonine Kinase 17b (STK17B) Kits ELISA

Human serine/threonine Kinase 17b (STK17B) interaction partners

1. STK17B promotes carcinogenesis and metastasis via AKT/GSK-3beta/Snail signaling in hepatocellular carcinoma.

2. A significant interaction between variants in STK17B and PAX8, in papillary thyroid cancer susceptibility, is reported.

3. ChIP assays showed that in U937 cells MYB binds to a conserved element upstream of the DRAK2 transcription start site.

4. DRAK2 protein directly binds to the type I TGF-beta receptor and Knockdown of DRAK2 suppresses the tumorigenic ability of breast cancer cells.

5. DRAK2 and protein kinase D form a novel signaling module that controls calcium homeostasis following T cell activation.

6. DRAK2 kinase activity is regulated in a calcium-dependent manner and that Ser(12) phosphorylation is necessary for optimal suppression of T cell activation by this kinase

7. Strong suppression of T cell receptor signals during thymic selection caused by ectopic DRAK2 expression in a DRAK2 transgenic mouse model of autoimmune encephalomyelitis alters the responsiveness of peripheral T cells.

8. Regulation of the apoptosis-inducing kinase DRAK2 by cyclooxygenase-2 in colorectal cancer.

Mouse (Murine) serine/threonine Kinase 17b (STK17B) interaction partners

1. Data provide insight into the role of Drak2 in autoimmune diseases by showing that Drak2 may not suppress TGF-beta signaling in T cells, and therefore may contribute to autoimmune disease via other molecular pathways.

2. does not function as an essential tumor suppressor or tumor surveillance protein

3. results demonstrate that DRAK2 plays an important role in primary and memory T cell responsiveness to allografts

4. DRAK2 and protein kinase D form a novel signaling module that controls calcium homeostasis following T cell activation.

5. T cells from Drak2(-/-) mice exhibited enhanced sensitivity to T cell receptor-mediated stimulation with a reduced requirement for costimulation

6. DRAK2 transduces non-apoptotic signals during thymocyte differentiation.

7. Drak2 expresses in the T cell compartment but is not T cell-specific; it plays critical roles in T cell apoptosis and memory T cell development

8. DRAK2 kinase activity is regulated in a calcium-dependent manner and that Ser(12) phosphorylation is necessary for optimal suppression of T cell activation by this kinase

9. DRAK2 may be a novel target for stimulating protective immunity to viral pathogens

10. DRAK2 may have a role in regulating the GC reaction and the response to thymus-dependent antigens, and DRAK2-deficiency is not involved in regulating intrinsic B-cell apoptosis.

11. reduced viral load in the brains of Drak2(-/-) mice

12. Drak2 overexpression led to aggravated beta-cell apoptosis triggered by free fatty acids (FFA) by compromising the increase of anti-apoptotic factors, such as Bcl-2, Bcl-xL and Flip, upon FFA assault

13. Drak2 regulates the survival of activated T cells and is required for organ-specific autoimmune disease

14. DRAK2 blockade may lead to permanent autoimmune T cell destruction via intrinsic apoptosis pathways.

15. p70S6 kinase was a bona fide Drak2 substrate